Microcystin-RR (MC-RR) has been suggested to induce apoptosis in tobacco BY-2 cells through mitochondrial dysfunction including the loss of mitochondrial membrane potential (Delta Psi(m)). To further elucidate the mechanisms involved in MC-RR induced apoptosis in tobacco BY-2 cells, we have investigated the role of mitochondrial electron transport chain (ETC) as a potential source for reactive oxygen species (ROS). Tobacco BY-2 cells after exposure to MC-RR (60 mg/L) displayed apoptotic changes in association with an increased production of ROS and loss of Delta Psi(m). All of these adverse effects were significantly attenuated by ETC inhibitors including Rotenone (2 mu mol/L, complex I inhibitor) and antimycin A (0.01 mu mol/L, complex III inhibitor), but not by thenoyltrifluoroacetone (5 mu mol/L, complex II inhibitor). These results suggest that mitochondrial ETC plays a key role in mediating MC-RR induced apoptosis in tobacco BY-2 cells through an increased mitochondrial production of ROS. (C) 2014 The Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences. Published by Elsevier B.V.